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Astaxanthin (ATX), the most abundant flavonoids in propolis, has been proven to exert neuroprotective property against cerebral ischemiainduced apoptosis.However, the mechanisms by which ATX mediates its therapeutic effects in vitro are unclear.In the present study, the article explored the underlying mechanisms involved in the protective effects of ATX via the PI3K/Akt/GSK3β/Nrf2 signaling pathway in SHSY5Y cells.For study of mechanism, the phosphoinositide 3 kinase (PI3K)Akt inhibitor LY294002, Glycogen synthase kinase 3β(GSK3β) inhibitor LiCl were used.Pretreatmentwith ATX for 24h significantly reduced the OGD induced viability loss, apoptotic rate and attenuated OGDmediated ROS production.In addition, ATX inhibited OGDinduced mitochondrial membrane potential, decreased Bcl2/Bax ratio.PI3K/Akt/GSK33/Nrf2 signaling pathway activation in SHSY5Y was tested by Western blot.Nrf2 expression was increasing by ATX and counteracted by PI3K/Akt inhibitor LY294002, GSK3β inhibitor LiCl in SHSY5Y.Nrf2 Immunocytochemistry showed Nrf2 nuclear translocation was increasing by ATX and counteracted by LY294002 or LiCl in SHSY5Y, respectively.It may be suggested that astaxanthin against cerebral ischemiainduced apoptosis in vitro via a programmed PI3K/Akt/GSK3β/Nrf2 signaling pathway in vitro.